Studies of the B19 parvovirus can be separated into clinical and basic laboratory work. In the laboratory, interesting molecular features of the B19 parvovirus have been elucidated using in vitro transcription and translation systems. We have identified the precise relationship between specific virus transcripts and protein products and demonstrated that multiple upstream AUG triplets help to regulate the quantities of viral capsid protein produced. A major problem in B19 parvovirus studies has been the lack of a simple, productive culture system for production of antigen. This difficulty has been overcome by creation of a viral capsid- producing cell line. Chinese hamster ovary cells have been transfected with DNA from the right side of the B19 genome. These cells produce B19 parvovirus empty capsids as well as large quantities of the major and minor capsid species. Clinical studies have demonstrated that B19 parvovirus replicates in cells of the peripheral blood during acute infection. B19 persistence has been shown in ar least three patient populations patients with congenital immunodeficiency, children with acute lymphocytic leukemia in remission on chemotherapy, and patients with acquired immunodeficiency syndrome. A common immunologic finding in patients with persistent disease is the absence of neutralizing antibody, which is paralleled by a low or absent binding of serum to virus capsid proteins on Western immunoblot analysis. Patients with persistent B19 parvovirus infection usually manifest their illness only by chronic red cell aplasia. The diagnosis may be established clinically based on characteristic bone marrow morphology and then confirmed by appropriate DNA studies. One patient with at least a three and probably as long as 12 year course of chronic parvovirus infection has been "cured" by the infusion of commercial immunoglobulin containing antibodies to parvovirus.